Do SARMs Cause Hair Loss? | Can SARMs Prevent Hair Loss?

Do SARMs Cause Hair Loss?

One of the first questions many have regarding SARMs is “Do SARMs cause hair loss?”

All SARMs can cause hair loss.

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The extent to which they can cause it is based upon their own inherent tissue selectivity and androgenicity.

There is no SARM as of now that is completely selective for anabolic to androgenic activity in the body.

All SARMs Can Be Androgenic

Some dosage for every SARM no matter which it is will induce prostate growth, which in turn will likely have an effect on the hair follicles on your head, facial hair growth, and other virilization side effects.

Typically, if somebody starts losing hair on SARMs it is the result of telogen effluvium, or using a high dosage of SARM way beyond what the probable therapeutic dosage would be established at.

How SARMs Can Prevent Hair Loss

While SARMs can cause hair loss, they can also prevent hair loss.

At least in theory they can prevent hair loss, as there is no clinical study to assess this specifically.

Anecdotally, if you reverse engineer how SARMs work you can see how they’re going to play out in a hair loss prevention context.

I personally know a few individuals who actually do this for their hair loss prevention protocols in conjunction with oral Estradiol to maintain healthy E2 levels.

SARMs were created to replace the therapeutic anabolic benefits of testosterone on muscle tissue and bone.

The dosage at which many SARMs in clinical development fulfill and hit that threshold of therapeutic activity not only suppress the endogenous production of testosterone, but they compete with Testosterone and DHT for the androgen receptor (AR).

By suppressing systemic Testosterone levels in the body and competing with Testosterone and DHT for the androgen receptor, androgenic activity in the body is substantially decreased.

This reduces prostate size and can potentially also reduce hair loss.

How SARMs Suppress Testosterone Levels

SARMs suppress the endogenous production of luteinizing hormone and follicle-stimulating hormone, which in turn lowers natural testosterone production.

The result of this is a suppression of the endogenous androgens that progress androgenic alopecia.

How SARMs Compete With Testosterone And DHT

SARMs were designed to have a very strong binding affinity.

Hundreds of SARMs have been synthesized over the years.

Some have a much higher binding affinity than others.

Throughout the years, a handful of SARMs have been developed that exhibit a binding affinity superior to Testosterone, and formidable to DHT.

When a SARM with a high binding affinity enters the body and starts occupying androgen receptors, there will be less vacant androgen receptors for Testosterone and DHT to bind to.

If Testosterone and DHT cannot bind to the androgen receptor, they cannot mediate their anabolic and androgenic effects in the body.

Preclinical models have proven that SARMs can antagonize the androgenic effects of Testosterone by competing for androgen receptor binding, while concurrently enhancing the overall anabolic effects in muscle tissue.

Essentially, when an efficacious SARM is introduced into the body, it binds to androgen receptors with a formidable or greater affinity than the body’s natural endogenous androgens (Testosterone and DHT), and then facilitates its tissue selective anabolic effects, which ultimately prevents many of the negative androgenic side effects of Testosterone and DHT (because they are being outperformed by the SARM in binding affinity), while simultaneously inducing maximal anabolic activity in muscle tissue and bone.

This is exhibited in a preclinical rodent model conducted using Testosterone Propionate and RAD140.

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In the study, Testosterone on its own built less muscle and induced more androgenic activity than the same dosage of Testosterone did with RAD140 [R].

In a sense, SARMs act similarly to systemic antiandrogens, except they won’t destroy the body because they mediate their own anabolic effects in muscle and bone as effectively as Testosterone, while sparing androgen-affected tissues of any significant stimulation.

In the near future, I’m sure we can expect to see increasingly effective SARMs with stronger binding affinities and even better tissue selectivity.

SARMs Vs Finasteride Efficacy For Hair Loss Prevention

This is where SARMs get even more interesting in a hair loss prevention context. S1 was one of the first SARMs ever synthesized.

It was abandoned in preclinical trials because it was not nearly as effective as some of the newer SARMs that are in stage 2 clinical trials now like LGD-4033 and Ostarine.

A preclinical rodent model assessed how effective S1 is at suppressing benign prostatic hyperplasia compared to Finasteride [R].

Finasteride was created for this exact purpose (reducing prostate size), but the makers of the drug figured out that suppressing DHT levels indirectly also reduces hair loss.

Off-label it was prescribed for hair loss prevention as well, and then eventually Propecia was created, which is the official brand name of Finasteride prescribed for hair loss prevention.

Hair loss prevention with Finasteride is indirectly caused by a suppression of endogenous androgens via dropping DHT, which ultimately lowers prostate size.

S1 was compared to Finasteride and Hydroxyflutamide in this study.

At all dosages tested S1 outperformed Finasteride in efficacy measures.

Not only did S1 reduce prostate size more than Finasteride (which decreases hair loss miniaturization), it also induced a greater amount of anabolic activity than Finasteride.

This means that S1 could sustain the physiological functions fulfilled by Testosterone in muscle tissue and bone with a lower androgen load on the body, and theoretically less hair loss.

Keep in mind that S1 is a first generation SARM, and more efficacious SARMs were discovered thereafter, which is why it was eventually abandoned.

Some of the newer stronger SARMs would perform even more favorably than S1 did in the same context.

SARMs Usage In Humans To Prevent Hair Loss?

The more tissue selective of a compound used on a research subject, the more efficacious it is for potential hair loss prevention.

Let’s just say you have a SARM with 500 to 1 anabolic to androgenic ratio of selectivity and a very high binding affinity.

Testosterone’s anabolic to androgenic ratio is 1 to 1.

With the SARM, you could theoretically keep muscle tissue and bone maintenance at therapeutic levels while simultaneously nuking testosterone and DHT via the suppression of natural testosterone level in the body.

The SARM would also occupy androgen receptors with a greater affinity than Testosterone and DHT, which would prevent AR mediated androgenic activity to a large extent.

Concurrently while those two things are happening, you indirectly reduce hair follicle miniaturization.

Lower androgen index = decreased prostate size = decreased hair loss.

Reverse Engineering Androgenic Activity In The Body

On the opposite side of the spectrum, if you administered Proviron, Drostanolone, or literal DHT you would undoubtedly increase your prostate size, increase facial hair growth, increase body hair growth, and increase hair loss.

This is well known and accepted.

It is only logical that the exact opposite of injecting powerful androgens (lowering androgen activity at the AR) would have an exact opposite effect on the prostate and hair follicles as well.

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The goal is having as low of an androgen load while still fulfilling maximal anabolic functions in the body.

SARMs Cannot Be Used For HRT Without Estrogen

SARMs do not aromatize into Estrogen.

This is the inherent flaw of SARMs and is one of the main reasons why they will be disqualified as an effective hormone replacement therapy alternative.

When you suppress endogenous Testosterone and DHT significantly with high dosages of SARMs or long-term usage, you will also severely inhibit the production of the Testosterone, which is the hormone that aromatizes into Estrogen in the male body.

Estrogen is necessary for mediating healthy hair growth.

There are theories thrown around the internet that chronically elevated Estrogen levels cause hair loss.

By referring to the hormone profile of a healthy women (the gender that keeps their hair), we can clearly see that they have high Estrogen levels, Progesterone levels nearly equivalent to men two-thirds of the year (the full year with some forms of birth control), and low Testosterone/DHT levels.

On the other side of the spectrum, men have just enough Estrogen to fulfill physiological functions, nearly identical Progesterone levels to women the majority of the year, and high Testosterone/DHT levels.

Once you suppress Testosterone endogenously with a SARM, you eventually crush estrogen into the ground in parallel to your Testosterone and DHT being suppressed.

The only remedy for this would be oral or topical Estrogen administration to bring systemic Estrogen levels back up to where they should be.

In the context of male hormone replacement therapy, a doctor telling a guy to literally ingest Estrogen pills to bring their E2 levels up to where they should be is so far out of the realm of possibility, let alone SARMs making it into the context of a real HRT alternative prescription.

99% of doctors still don’t even understand how to properly prescribe TRT and safely optimize naturally occurring bioidentical hormones, so expecting them to understand and accept something this new and odd probably wouldn’t ever occur.

Future Alternatives To Traditional Hormone Replacement Therapy

I’m not advising anyone to do this, and this is all hypothetical.

I’m just talking about things I’ve noticed and that I find interesting in the space in terms of how things work in the body.

SARMs will inevitably greatly suppress Testosterone and DHT, as well as compete for androgen receptor activation, which may help prevent hair loss based on the clinical data.

Of course, this is all dependent on multiple factors, including if a mega dose of the SARM is being used or if it’s being used “therapeutic” amounts.

And then concurrent Estrogen administration to keep Estrogen levels where they should be would also be factored in.

This could all hypothetically drop androgen index in the body to a level that sustains a lack of hair loss miniaturization, mediates healthy hair growth with adequate estrogen levels, and simultaneously maintains adequate anabolic activity in the body with a lack of stimulation in androgen sensitive tissues.

I’m not sure why there weren’t more studies conducted on this specifically because it looks like a really promising area.

The S1 study in particular I have referenced before, and the data comparing other SARMs to Finasteride is even more promising.

As the scope broadens in terms of selective androgen receptor modulators and their potential therapeutic applications, I believe they will start being looked at in this potential context as well.

I see great potential in it, and I’ve seen a handful of real-world examples of people who have replicated this theory in their personal studies.

At the end of the day, hair loss in most cases boils down to what androgens are in the body, their binding affinity, their tissue selectivity, how they transcribe their effects and activate androgen receptors, their inherent androgenicity, and the total serum concentrations of them in the body.

Even if you have a very selective anabolic agent in the body (like a SARM), if a huge amount of it was circulating around, that could still be more than enough to induce prostate growth and hair loss.

Therefore, the answer to the question “do SARMs cause hair loss” is both yes and no.

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